The triggered mode of an implantable medical device (IMD), whether applied to the atrium or the ventricle involves delivery of a pacing stimulus/output in response to a sensed event. After the introduction of dual chamber pacing and sensing, devices with both triggered and inhibited mode functioning at the same time became available. The mode of response to a sensed event in a given chamber (for a triggered and inhibited mode device commonly identified as DDD) is to inhibit the output to the chamber in which the sensed event originated. In response to an event sensed in the atrium, the atrial output is inhibited and an AV delay is initiated. If a ventricular event is not detected within that interval, a ventricular output is triggered in response to the atrial paced or sensed event. This interval is the technologic equivalent of the intrinsic AV nodal conduction interval termed a PR interval when examining the surface electrocardiogram (ECG).
One of the limitations of the first generation of DDD pacemakers was the development of a pathologic atrial tachyarrhythmia that could be tracked by the pacemaker resulting in sustained high rate ventricular pacing. This was first managed by limiting the maximum tracking rate. With the incorporation of rate modulation in DDD pacemakers, manufacturers allowed independent programming of the maximum tracking rate (MTR) and the maximum sensor rate (MSR) where the MSR could be programmed to a rate that was faster than the MTR allowing a higher rate during a physiologic stress such as exercise. The next improvement was the development of a variety of automatic mode switch (AMS) algorithms. These would recognize the pathologic atrial tachyarrhythmia and cause an internal mode switch from a tracking mode (DDD) to a non-tracking mode (VVI or DDI). If there was otherwise intrinsic AV nodal conduction, the pacemaker would be inhibited while the atrial tachyarrhythmia was present. If there was concomitant AV block, the pacemaker would provide ventricular pacing but in a non-tracking mode and hence provide base rate pacing that might be different than the base rate during DDD function or a rate defined by sensor activity (rate modulation). With the introduction of cardiac resynchronization therapy (CRT) where ventricular pacing was specifically desired to provide a more synchronous ventricular activation and contraction pattern, the development of an atrial tachyarrhythmia resulting in AMS, the normal tracking mode reverts to a non-tracking mode, e.g., single chamber, ventricular sensing and pacing in the inhibited mode (VVI) or dual chamber pacing and sensing in the inhibited mode (DDI). This implementation results in inhibition of the ventricular output as long as there is intact conduction resulting in the loss of cardiac resynchronization. Brief episodes of an atrial tachyarrhythmia that are sufficiently rapid to trigger AMS, most commonly atrial fibrillation, have limited adverse effects. However, protracted episodes may significantly compromise the benefits associated with CRT as it functionally disables CRT when AV nodal conduction is intact.
In an effort to address the limitations of prior techniques, manufacturers have introduced the triggered mode to be active during AMS with the desire to maintain the maximal degree of resynchronization possible.
Current generations of high voltage devices generally sense on the right ventricle (RV) channel, although some devices enable left ventricle (LV) signal amplitude measurements. Such left ventricle sensing may be for the purpose of detecting rapid ventricular rates for the potential delivery of anti-tachycardia pacing and/or high voltage therapy. In the original parallel output biventricular (CRT) defibrillators, both the right ventricle and left ventricle activations could be sensed if the second input signal to the sensing circuit occurred after completion of the ventricular refractory period initiated by either the ventricular pacing output or the first sensed component of the ventricular electrogram. This could result in a normal intrinsic or ventricular paced rhythm being interpreted as ventricular tachycardia (VT) or ventricular fibrillation (VF) resulting in the delivery of inappropriate high voltage therapy. As such, most current devices detect only in the right ventricle or in only a single ventricular chamber to eliminate the problem of double counting.
The majority of individuals who receive a CRT system for management of heart failure have a wide intrinsic QRS complex [>120 ms in duration] that is most commonly a left bundle branch block (LBBB) pattern. This means that the earliest intrinsic ventricular activation is on the right side of the heart with the impulse crossing the interventricular septum to begin to activate the left ventricle. This interventricular activation interval is commonly 100 ms or longer. The goal of triggered pacing in a CRT system is to detect intrinsic ventricular activation and then deliver an output pulse as soon after the detected signal as possible to restore some degree of synchronization. In the current generation CRT systems, the output is delivered to both leads which means that output to the RV (because sensing only occurs in the RV) will be wasted as that chamber has already been depolarized. If the signal sensed in the RV originated from the LV, the output pulse to the LV will also be ineffective as that chamber will have already been depolarized.
In addition, many patients with heart failure who would qualify for a CRT system also have frequent premature ventricular complexes (PVCs) which serve to inhibit the pacemaker. The triggered mode could theoretically improve coordination (resynchronization) in association with isolated PVCs. However, if the PVCs arise in the left ventricle as is very common, by the time that it reaches the right ventricle in order to be sensed, both chambers will be fully depolarized and will be refractory to pacing. As such, the triggered mode in this situation is wasting energy without contributing a hemodynamic benefit.
More recent CRT systems have allowed for the independent programmability of left ventricle and right ventricle stimulation and the timing between the two outputs. This allows for adjustment of the inter-ventricular conduction (V-V) interval. In the majority of patients, the general recommendation is for sequential rather than simultaneous pacing with the left ventricle usually stimulated before the right ventricle. With sensing restricted to the right ventricle, delivery of a triggered stimulus to the left ventricle (presuming that the electrical activation also started in the RV) results in right ventricle activation prior to left ventricle activation even if the interventricular conduction delay is minimized.
In patients who have frequent PVCs, particularly arising from the left ventricle as well as a right bundle branch block pattern associated with intrinsic AV nodal conduction, triggered pacing offers little benefit because by the time the intrinsic activation is detected, both chambers will have been depolarized. Therefore, it is desirable to provide a system or method that improves on the current triggered mode technology to help restore CRT in the presence of intrinsic conduction during automatic mode switch or in association with isolated ventricular ectopic beats or PVCs.
Individuals with heart failure and atrial tachyarrhythmias commonly have inter-atrial conduction defects. It has been shown that bi-atrial or dual-site atrial pacing can improve atrial depolarization and reduce the frequency of atrial tachyarrhythmias. At the present time, there are no commercially available pulse generators designed for bi-atrial pacing or four chamber pacing in the presence of concomitant CRT. When there is dual-site atrial pacing; be this two sites in the right atrium or right atrium and left atrium, triggered pacing may also improve both electrical and hemodynamic atrial resynchronization. Similar to CRT in the ventricles, triggered mode pacing may be effective in the atrium in the presence of an intrinsic rhythm such as sinus where the sensed P wave, be this sinus, an ectopic atrial rhythm or isolated atrial premature beats thus improving hemodynamics and reducing the incidence of atrial tachyarrhythmias. Should the patient develop an atrial tachyarrhythmia defined as an atrial rate above a programmed value in pulse per minute or a filtered atrial rate interval shorter than a programmable interval in milliseconds, triggered mode pacing in the atrium will be suspended.